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Migraine Aura (migraine + aura)

Distribution by Scientific Domains

Medical Sciences	85%

Selected Abstracts

Effect of cortical spreading depression on synaptic transmission of rat hippocampal tissues

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 5 2006
Brigitta Wernsmann
Abstract Cortical spreading depression (CSD) is believed to be a putative neuronal mechanism underlying migraine aura and subsequent pain. In vitro and ex vivo/in vitro brain slice techniques were used to investigate CSD effects on the field excitatory postsynaptic potentials (fEPSP) and tetanus-induced long-term potentiation (LTP) in combined rat hippocampus,cortex slices. Induction of CSD in combined hippocampus,cortex slices in which DC negative deflections did not propagate from neocortex to hippocampus significantly augmented fEPSP amplitude and LTP in the hippocampus. Propagation of CSD to the hippocampus resulted in a transient suppression followed by reinstatement of fEPSP with amplitude of pre-CSD levels. LTP was inhibited when DC potential shifts were recorded in the hippocampus. Furthermore, CSD was induced in anaesthetized rats and, thereafter, hippocampal tissues were examined in vitro. LTP was significantly enhanced in hippocampal slices obtained from ipsilateral site to the hemisphere in which CSD was evoked. The results indicate the disturbances of hippocampal synaptic transmission triggered by propagation of CSD. This perturbation of hippocampal synaptic transmission induced by CSD may relate to some symptoms occurring during migraine attacks, such as amnesia and hyperactivity. [source]

Brain Apparent Water Diffusion Coefficient Magnetic Resonance Image During a Prolonged Visual Aura

HEADACHE, Issue 6 2010
Robert Belvís MD
(Headache 2010;50:1045-1049) Background., Reversible changes in brain magnetic resonance imaging (MRI) weighted in diffusion-weighted images (DWI) and apparent water diffusion coefficient (ADC) maps have been reported in acute stroke, epilepsy, eclampsia, and hypoglycemia, but they are contradictory regarding to migraine aura. Objective., A 41-year-old woman with known basilar migraine for 5 years consulted about a persistent visual aura (visual snow phenomenon) plus bilateral paresthesias in the extremities for 4 days. The headache was treated with success with 10 mg of wafer rizatriptan and 600 mg of ibuprophen. Methods., The neurologic and ophthalmologic examination were normal. An urgent brain MRI detected no lesions in T1, T2, fluid-attenuated inversion recovery, and DWI, but an abnormal signal appeared in the left occipital lobe in ADC and (r)ADC maps. The brain MRI angiography, carotid ultrasound study, transesophageal echocardiography, 24-hour cardiac Holter monitoring, and thrombophilia study were normal. Results., A new brain MRI 8 days after did not show any previous lesion in the same sequences. Conclusions., We present a patient with migraine and transitory abnormal signals in the ADC map of an occipital region during persistent visual aura. The clinical-radiological relationship is congruent. Some similar cases have showed these MRI signals during the aura, suggesting cytotoxic edema, without ischemic lesions in the MRI controls. Theses ADC images probably appear in complex auras. [source]

Caliber Fluctuations of Cervical Internal Carotid Artery and Migraine With Aura: A Possible Vasospasm Detected by Ultrasonographic Examinations

HEADACHE, Issue 7 2009
Susanna Usai MD
Caliber fluctuations of extra- and intracranial arteries, mostly related to vasospasm, are often recognized in various neurological conditions. We report a case of a 33-year-old woman affected by migraine with and without aura who exhibited a possible cervical internal carotid artery vasospasm, detected by ultrasound, before a typical migraine aura. [source]

Microemboli may link spreading depression, migraine aura, and patent foramen ovale

ANNALS OF NEUROLOGY, Issue 2 2010
Ala Nozari MD
Objective Patent foramen ovale and pulmonary arteriovenous shunts are associated with serious complications such as cerebral emboli, stroke, and migraine with aura. The pathophysiological mechanisms that link these conditions are unknown. We aimed to establish a mechanism linking microembolization to migraine aura in an experimental animal model. Methods We introduced particulate or air microemboli into the carotid circulation in mice to determine whether transient microvascular occlusion, insufficient to cause infarcts, triggered cortical spreading depression (CSD), a propagating slow depolarization that underlies migraine aura. Results Air microemboli reliably triggered CSD without causing infarction. Polystyrene microspheres (10,m) or cholesterol crystals (<70,m) triggered CSD in 16 of 28 mice, with 60% of the mice (40% of those with CSD) showing no infarcts or inflammation on detailed histological analysis of serial brain sections. No evidence of injury was detected on magnetic resonance imaging examination (9.4T; T2 weighted) in 14 of 15 selected animals. The occurrence of CSD appeared to be related to the magnitude and duration of flow reduction, with a triggering mechanism that depended on decreased brain perfusion but not sustained tissue damage. Interpretation In a mouse model, microemboli triggered CSD, often without causing microinfarction. Paradoxical embolization then may link cardiac and extracardiac right-to-left shunts to migraine aura. If translatable to humans, a subset of migraine auras may belong to a spectrum of hypoperfusion disorders along with transient ischemic attacks and silent infarcts. ANN NEUROL 2010;67:221,229 [source]

Androgenic suppression of spreading depression in familial hemiplegic migraine type 1 mutant mice,

ANNALS OF NEUROLOGY, Issue 4 2009
Katharina Eikermann-Haerter MD
Familial hemiplegic migraine type 1 (FHM1), a severe migraine with aura variant, is caused by mutations in the CACNA1A gene. Mutant mice carrying the FHM1 R192Q mutation exhibit increased propensity for cortical spreading depression (CSD), a propagating wave of neuroglial depolarization implicated in migraine aura. The CSD phenotype is stronger in female R192Q mutants and diminishes after ovariectomy. Here, we show that orchiectomy reciprocally increases CSD susceptibility in R192Q mutant mice. Chronic testosterone replacement restores CSD susceptibility by an androgen receptor-dependent mechanism. Hence, androgens modulate genetically-enhanced CSD susceptibility and may provide a novel prophylactic target for migraine. Ann Neurol 2009;66:564,568 [source]